Abstract
Prostate cancer (PCa) is a leading cause for death in men and the most commonly diagnosed malignancy globally. MicroRNA (miR)‑583 expression levels have been discovered to be downregulated in recurrent PCa samples compared with non‑recurrent cases. However, the precise functions and pathogenic mechanism of miR‑583 in the development of PCa are vague, thus the aim of the present study was to investigate these. The expression levels of miR‑583 and Janus kinase 1 (JAK1) in PCa tissues and cell lines were analyzed using reverse transcription‑quantitative PCR and western blotting. The protein expression levels of phosphorylated (p)‑STAT3 and STAT3 in PCa cell lines were also analyzed using western blotting. The effects of miR‑583 and JAK1 on the proliferation and invasion of PCa cell lines cell lines were determined using MTT and Transwell assays, respectively. The binding interaction between miR‑583 and the 3'‑untranslated region of JAK1 were predicted by TargetScan, and further validated using dual luciferase reporter assays in PCa cell lines. The results revealed that the expression levels of miR‑583 were downregulated, while those of JAK1 were upregulated in PCa tissues and cell lines (DU145 and PC3). The transfection with the miR‑583 mimic inhibited the proliferation and invasion, as well as downregulating JAK1 and p‑STAT3 protein expression levels in DU145 and PC3 cell lines. These effects were partially abolished following the overexpression of JAK1. Moreover, JAK1 was identified to be a target gene for miR‑583 in DU145 and PC3 cell lines and the expression levels of miR‑583 were revealed to be negatively correlated with JAK1 expression levels in PCa tissues. In conclusion, the findings of the present study suggested that miR‑583 may inhibit the proliferation and invasion of PCa cells by targeting JAK1, thus providing a novel therapeutic target for patients with PCa.